Christie A Flanagan1, Kathryn R Koller2, Abbie W Wolfe2, Timothy K Thomas2, Neal L Benowitz3,4, Caroline C Renner2, Christine Hughes5, Dorothy K Hatsukami6, Carrie Bronars5, Neil J Murphy7, Gretchen Day2, Paul A Decker8, Christi A Patten5. 1. Clinical and Research Services, Division of Community Health Services, Alaska Native Tribal Health Consortium, Anchorage, AK; caflanagan@anthc.org. 2. Clinical and Research Services, Division of Community Health Services, Alaska Native Tribal Health Consortium, Anchorage, AK. 3. Center for Tobacco Control Research and Education, University of California, San Francisco, CA. 4. Division of Clinical Pharmacology and Experimental Therapeutics, Medical Service, Departments of Medicine, and Bioengineering and Therapeutic Sciences, University of California, San Francisco, CA. 5. Department of Psychiatry and Psychology, Mayo Clinic, Rochester, MN. 6. Department of Psychiatry, University of Minnesota, Minneapolis, MN. 7. Southcentral Foundation, Department of Obstetrics and Gynecology, Alaska Native Medical Center, Anchorage, AK. 8. Divison of Biomedical Statistics and Informatics, Mayo Clinic, Rochester MN.
Abstract
INTRODUCTION: The high prevalence of smoking and smokeless tobacco (ST) use during pregnancy in Alaska Native (AN) women is concerning due to the detrimental effects of these products to the mother and the developing fetus. We sought to correlate maternal cotinine levels with fetal exposure to a tobacco-specific carcinogen to incorporate in a biomarker feedback intervention to motivate tobacco cessation during pregnancy. METHODS: Demographic and tobacco use data were collected from a convenience sample of pregnant AN smokers, ST users, and non-users. Maternal and neonatal urine were collected at delivery. Maternal urine cotinine and neonatal urine total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL, a tobacco-specific carcinogen) levels in smokers and ST users were analyzed and their correlations determined by Spearman correlation coefficients. RESULTS: During 2012-2014, we enrolled 64 non-users, 54 smokers, and 30 ST (20 homemade iqmik; 10 commercial ST) users (n = 148). Analyses of paired maternal-infant urine samples obtained for 36 smokers demonstrated a moderate to strong correlation (r = 0.73, P < .001) between maternal cotinine and infant NNAL levels. The correlation was not significant for 25 iqmik users (r = 0.36, P = .17) or 9 commercial ST users (r = 0.60, P = .09). No analysis was conducted for 55 non-users with cotinine and NNAL levels < limits of quantification. CONCLUSIONS: There is a moderate to strong correlation between maternal smoking and fetal exposure to the tobacco-specific carcinogen NNAL. IMPLICATIONS: The correlation between maternal smoking and fetal carcinogen exposure may provide an education tool to help motivate smoking cessation among pregnant AN women. Further investigation is warranted to determine correlations between maternal commercial ST and iqmik use and neonatal NNAL.
INTRODUCTION: The high prevalence of smoking and smokeless tobacco (ST) use during pregnancy in Alaska Native (AN) women is concerning due to the detrimental effects of these products to the mother and the developing fetus. We sought to correlate maternal cotinine levels with fetal exposure to a tobacco-specific carcinogen to incorporate in a biomarker feedback intervention to motivate tobacco cessation during pregnancy. METHODS: Demographic and tobacco use data were collected from a convenience sample of pregnant AN smokers, ST users, and non-users. Maternal and neonatal urine were collected at delivery. Maternal urine cotinine and neonatal urine total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL, a tobacco-specific carcinogen) levels in smokers and ST users were analyzed and their correlations determined by Spearman correlation coefficients. RESULTS: During 2012-2014, we enrolled 64 non-users, 54 smokers, and 30 ST (20 homemade iqmik; 10 commercial ST) users (n = 148). Analyses of paired maternal-infant urine samples obtained for 36 smokers demonstrated a moderate to strong correlation (r = 0.73, P < .001) between maternal cotinine and infantNNAL levels. The correlation was not significant for 25 iqmik users (r = 0.36, P = .17) or 9 commercial ST users (r = 0.60, P = .09). No analysis was conducted for 55 non-users with cotinine and NNAL levels < limits of quantification. CONCLUSIONS: There is a moderate to strong correlation between maternal smoking and fetal exposure to the tobacco-specific carcinogen NNAL. IMPLICATIONS: The correlation between maternal smoking and fetal carcinogen exposure may provide an education tool to help motivate smoking cessation among pregnant AN women. Further investigation is warranted to determine correlations between maternal commercial ST and iqmik use and neonatal NNAL.
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